18.07.2021 – 12:45
Like all living organisms, viruses have their own life cycles. They are parasitic, starting at the moment when a parent virus infects another creature and invades its cells to make copies of itself.
In the case of SARS-CoV-2, the virus that is causing the current pandemic, this happens when the virus penetrates through an enzyme called ACE2 into the membrane of some human cells, and slides into its genome. This cell invasion is aided by a protein that studies the surface of the virus.
Changes in this protein, driven by genetic changes due to mutation, also change the general properties of the virus, and especially its ability to spread through populations. The changing nature of viruses has its source in the natural coincidence that occurs within the process of producing copies of each object, making them unavoidable.errors, which are called mutations.
The vast majority of viruses cannot survive mistakes in the breeding process.
But some do, and may even thrive as a result of these changes, gaining competition with ancestral viruses, and spreading to a more efficiently through their host population.
There are some parts of the structure of the virus that are best able to withstand mutations: the protein that coats the outside of the virus is more tolerant of change. Viruses that undergo mutations and survive are called variants. They started appearing on November last year, with the Alpha variant that was first discovered in Kent, in the south-east of England.
New variants, must have priority over the old ones, if they become the dominant form of the virus.
One of the first mutations since increases transmittance was known as N501Y or “Nelly”, a of the eight mutations that characterized the viral protein of the Alpha variant. The technical name of the mutation refers to changes in the virus genome. “501” means that change is occurring in amino acid 501 in a chain of 1,273 of such as constitute the viral protein.
Since different amino acids have slightly different chemical properties, this one change has an impact on the structure of the envelope protein.
As a result, the way electricity is distributed changes. This in turn slightly changes the shape of the protein, as positively charged areas attract negatively charged areas. Thanks to this dynamic, the N501Y allows a substantial portion of the roof to rotate about 20 degrees, making it fit better with the ACE2 receptor.
This increases transmissibility. Other mutations perform a similar trick Delta, the variant that was first discovered in India and is currently spreading around the world, seems to be even more transmissible than Alpha and other variants. Although it is not clear, as detailed structural studies on the protein of this variant have not yet been completed.
But Ravindra Gupta, a molecular virologist at Cambridge University, and his colleagues argue that Delta’s increased transmittance is partly due to a mutation in the amino acid no.681 site. This is the point at the top where it binds to ACE2, and the viral protein cleaves on two.
Meanwhile, there are other theoretical mutations that make the virus more transmissible and which it has not yet achieved. But there are others that help it avoid the antibodies released by the immune system in order to protect the body from infection.
